The consensus conference on cardio-renal syndromes (2008) defined ‘cardio-renal syndromes’ as ‘disorders of
the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the
other’ and identified five subtypes of the syndromes. Various pathophysiologic mechanisms underlie cardiorenal syndrome
including hemodynamic derangements, reduced cardiac output leading to impaired renal perfusion, reduced stroke
volume, raised atrial filling pressures, elevated atrial pressures, sodium and water retention, venous congestion, right
ventricular dysfunction and venous hypertension causing increased renal venous pressure, intra-abdominal hypertension,
various neurohormonal adaptations including activation of the renin-angiotensin-aldosterone system, adaptive activation
of the sympathetic nervous system, cytokine release and oxidative stress. Although there are standardized clinical
guidelines for the management of heart failure, and chronic kidney disease, respectively, there are no similar consensus
clinical guidelines for the management of the cardiorenal syndromes.
RAAS inhibition is advocated in treating systolic heart failure. There is evidence that RAAS inhibition is also useful in
cardiorenal syndrome. However, RAAS inhibition, while potentially useful in the management of cardiorenal syndrome,
is not the ‘magic bullet’, is sometimes limited by adverse renal events, is not applicable to all patients, and must be applied
by physicians with due diligence and caution. Nevertheless, a more comprehensive multidisciplinary multipronged approach
to managing patients with cardiorenal syndrome is even more pragmatic and commonsense given the multiple
mechanisms and pathogenetic pathways implicated in the causation and perpetuation of cardiorenal syndrome.